Obesity and its associated comorbid conditions are among the most prevalent and challenging conditions confronting the medical profession in the 21st century. Estimates by the World Health Organization indicate that over 1.7 billion people worldwide are overweight (BMI≥25) or obese (BMI≥30) with over 2.5 million deaths annually attributable to obesity. In the U.S., adult obesity rates rose from 14% in 1978 to over 30% in 2000 with over 50% of Americans projected to be obese in 2030. Common comorbidities of over-nutrition and obesity include insulin resistance and the development of hepatic steatosis (i.e., nonalcoholic fatty liver disease, which is noted in about 75% of obese patients). However, the mechanisms responsible for obesity and other metabolic sequelae associated with overconsumption of dietary fats are poorly understood.
The small intestine plays a central role in the control of energy homeostasis through the digestion, absorption and assimilation of ingested nutrients. Food ingestion is associated with the increased secretion of multiple gut peptides, produced in specialized enteroendocrine cells scattered along the length of the small bowel, that act on distant target sites (e.g., liver, muscle and adipose tissue) to promote the efficient uptake and storage of energy, and the regulation of lipid and glucose homeostasis. While GI hormones can regulate energy balance in a number of ways, the role that gut hormones play in obesity and metabolic disorders is poorly understood.
Accordingly, methods for predicting increased risk of obesity in non-obese subjects is desirable.